Type 2 inflammation contributes to skin barrier dysfunction in atopic dermatitis

Skin barrier dysfunction, a defining feature of atopic dermatitis (AD), arises from multiple interacting systems. In AD, skin inflammation is caused by host–environment interactions involving keratinocytes, as well as tissue-resident immune cells such as type 2 innate lymphoid cells, basophils, mast cells, and T-helper type 2 cells, which produce type 2 cytokines including interleukin (IL)-4, IL-5, IL-13, and IL-31. Type 2 inflammation broadly impacts expression of genes relevant for barrier function, such as intracellular structural proteins, extracellular lipids, and junctional proteins, and enhances Staphylococcus aureus skin colonization. Systemic anti-type 2 inflammation therapies may improve dysfunctional skin barrier in AD.